Angiotensin II converting enzyme inhibitor therapy has been shown to reduce protein excretion in several forms of glomerular disease. This diminution of protein excretion occurs in the presence and absence of systemic hypertension. In several experimental models of glomerular injury and progressive renal failure, glomerular hypertension is present in the absence of an elevated systemic arterial pressure. In most experimental models of renal injury, angiotensin II converting enzyme inhibitor therapy decreases glomerular hypertension, urinary protein excretion, and glomerular injury. In human studies the data are most compelling in patients with diabetic nephropathy. It is reasonably certain that glomerular hypertension plays a role in the pathogenesis of experimental diabetic nephropathy, and angiotensin II converting enzyme inhibitor therapy has a salutary effect. Several short term (<3 months), and long term (>6 months) studies have demonstrated that angiotensin II converting enzyme inhibitors reduce systemic blood pressure and proteinuria in diabetic patients. This therapy reduces proteinuria independent of the initial blood pressure or degree of pre-existing renal dysfunction. From our short term prospective trial, we know that an angiotensin II converting enzyme inhibitor is capable of reducing proteinuria in patients with sickle cell nephropathy for a short interval. An important question not answered by this short term study is whether or not angiotensin II converting enzyme inhibitor therapy, by reducing glomerular capillary hypertension, can ameliorate proteinuria for an extended time. An even more important question is whether or not angiotensin II converting enzyme inhibitor therapy can retard the progressive decline in renal function in sickle cell disease patients with renal insufficiency. Therefore, the questions that we wish to answer in the current study are whether the long term administration of an angiotensin II converting enzyme inhibitor in patients with sickle cell nephropathy: 1) prevents or retards the development of renal insufficiency, and 2) reduces proteinuria on a long term basis. Patients will be treated with either Enalapril or placebo. The primary outcome variable will be a change in the glomerular filtration rate.